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J. Petit-Jacques, S. A. Bloomfield; Multiple Synaptic Inputs Regulate Light-Dependent Oscillatory Currents in Starburst Amacrine Cells of the Mouse Retina. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4909.
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© ARVO (1962-2015); The Authors (2016-present)
To study the light responses of starburst amacrine cells in the mouse retina.
Patch clamp recordings were obtained from starburst amacrine cells visualized in the ganglion cell layer by infrared illumination, in a dark-adapted mouse retina-scleral preparation. The patch pipette solution contained biocytin, which allowed for subsequent morphological identification. Computer-generated light stimuli were produced by a DLP projector onto a coherent fiber optic and then delivered to the retina through the microscope objective.
Postsynaptic currents were usually recorded at a holding potential of -70 mV. The typical response of a starburst cell to small diameter spots of dim light (70 µm) consisted of a large ON transient peak of inward current followed by smaller amplitude oscillatory currents that lasted for the entire stimulus duration. Presentation of larger diameter stimuli (200 µm) reduced the amplitude of the response, presumably due to activation of a surround inhibition. The postsynaptic currents were apparently generated by activation of AMPA/kainate glutamate receptors, as they were virtually eliminated by application of 10 µM CNQX. The glutamate-activated currents were also abolished by application of extracellular cadmium, a non-specific blocker of calcium channels. Application of the metabotropic mGluR6 glutamate receptor agonist, DL-AP4, totally eliminated the light-evoked currents in starburst amacrine cells. This indicates that the glutamate was released from ON bipolar cells that synapse onto the displaced starburst amacrine cells. In the presence of the GABA receptors inhibitors, picrotoxin and biccuculline, the transient ON inward peak of current was enhanced in amplitude and the oscillatory currents showed both larger amplitude and half-width than under control conditions. Blockade of voltage-gated sodium channels with TTX increased the amplitude of the initial ON inward current, but eliminated the subsequent oscillatory currents. Finally, application of the specific glutamate transporter inhibitor, TBOA, increased the amplitude and duration of the initial ON inward current, but eliminated the subsequent oscillatory currents.
Our results indicate that the light-dependent transient and oscillatory currents in mouse starburst amacrine cells are dependent on glutamate release from presynaptic ON bipolar cells. In addition, inhibition from GABAergic and spiking amacrine cells also contribute to the shape of the light-dependent response of starburst amacrine cells, particularly the oscillatory component.
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